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Cancer and Angiogenesis

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Oncodynamics: Effects of Cancer Cells on the Body

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Abstract

Neoplastic growth is closely linked to neovascularization, as efficient blood supply is necessary to deliver oxygen and nutrients to a tumour. The development of blood vessels in tumours is modulated by pro- and anti-angiogenic factors. Pro-angiogenic factors include those that regulate remodelling of the extracellular matrix (ECM) and changes in perivascular cell structure, as well as those that promote endothelial cell changes and migration, including but not limited to vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and angiopoietin. Anti-angiogenic factors include thrombospondin, 16kDA N-terminal fragments of prolactin and growth hormone, endostatin, vasostatin, and angiostatin. During tumour growth, the balance is tipped in favour of pro-angiogenic factors. This is known as the angiogenic switch and allows for increased tumour progression, a state where proliferation is favoured over apoptosis. The angiogenic switch may thus be considered as the rate-limiting step in the tumour metastasis pathway. Furthermore, this switch is highly dependent on changes in the tumour microenvironment. The tumour microenvironment continues to increase in significance in angiogenesis research and understanding it holds the key to new and more successful anti-angiogenic cancer therapies.

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Abbreviations

ADM:

Adrenomedullin

Ang:

Angiopoetin

Akt:

Protein kinase B

APC:

Antigen-presenting cells

bFGF:

Basic fibroblast growth factor

CAF:

Cancer-associated fibroblasts

CCL2 CC:

Chemokine ligand 2

CSF-1:

Colony-stimulating factor-1

ECM:

Extracellular matrix

EGF:

Epidermal growth factor

EGFR:

Epidermal growth factor receptor

ERK:

Extracellular signal-regulated kinases

FAK:

Focal adhesion kinase

HER:

Human epidermal receptor

ICAM-1:

Intercellular adhesion molecule-1

IL1β:

Interleukin 1β

mCAF:

Mammary CAF

MDSC:

Myeloid-derived suppressor cell

MMP:

Matrix metalloproteinase

MT1-MMP:

Membrane-type1 matrix metalloproteinase

NF-κB:

Nuclear factor kappa-light-chain-enhancer of activated B cells

NK cells:

Natural killer cells

PA:

Tissue-type plasminogen activators

PAI-1:

PA inhibitior-1

PDGF:

Platelet-derived growth factor

PI3K:

Phosphoinositide 3-kinase

PlGF:

Placenta growth factor

PMP:

Platelet-derived microparticles

SDF-1:

Stromal cell-derived factor 1

TEM:

Monocytes expressing TIE-2 receptors

TGFα:

Transforming growth factor α

TGFβ-1:

Transforming growth factor β1

TME:

Tumour mircoenvironment

TNF-α:

Tumour necrosis factor α

TP:

Thymididine phosphorylase

Sema4D:

Semaphoring 4D

uPA:

Urokinase-type plasminogen activator

VCAM-1:

Vascular cell adhesion molecule-1

VEGF:

Vascular endothelial growth factor

VPF:

Tumour vascular permeability factor

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Authors and Affiliations

  1. Singh Lab, Department of Pathology and Molecular Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, Canada

    Franziska Miller

  2. Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada

    Gurmit Singh

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  1. Dept. Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada

    Gurmit Singh

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Miller, F., Singh, G. (2016). Cancer and Angiogenesis. In: Singh, G. (eds) Oncodynamics: Effects of Cancer Cells on the Body. Springer, Cham. https://doi.org/10.1007/978-3-319-28558-0_2

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